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Infective Endocarditis

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Presentation on theme: "Infective Endocarditis"— Presentation transcript:

1 Infective Endocarditis
DR. MOSTAFA ALSHAMIRI ASSOCIATE PROFESSOR CONSULTANT CARDIOLOGIST HEAD OF ADULT CARDIOLOGY Director of Coronary Care KING FAHED CARDIAC CENTER 341, KKUH October, 2018

2 AGENDA Definition Path-physiology The risk factors Clinical features
Diagnosis Treatment Complication Prevention

3 Infective Endocarditis
Definition : Infection of endothelium surface of heart either of 1. Heart valves . 2. Septal defects. 3. Chordae Tontine . 4. A.V shunt. It remains a life-threatening disease with significant mortality (about 20%) and morbidity.

4 Pathogenesis of IE-1 The IE is the net result of the complex interaction between the bloodstream pathogen with matrix molecules and platelets at sites of endocardial cells damage.

5 Pathogenesis of IE-2 Endothelial damage Turbulent blood flow produced by certain types of congenital or acquired heart disease, such as flow from a high- to a low-pressure chamber or across a narrowed orifice, traumatizes the endothelium. Formation of nonbacterial thrombotic endocarditis ( NBTE ) Endothelial damage creates a predisposition for deposition of platelets and fibrin on the surface of the endothelium, which results in NBTE. Bacteremia Invasion of the bloodstream with a microbial species that has the pathogenic potential to colonize this site ,then result in Proliferation of bacteria within a vegetation and form IE.

6 Pathogenesis of IE-3 Transient Bacteremia Mucosal surfaces are populated by : Dense endogenous microflora. Trauma to a mucosal surface like: Gingiva around teeth, Oro-pharynx, GI tract, Urethra, Vagina, This will releases many different microbial species transiently into the bloodstream which will leads to Transient bacteremia caused by organism e,g Veridans group streptococci

7 Pathogenesis: summery-1
1.High velocity jet 2.Flow from high pressure to low pressure chamber 3.Flow across narrow orifice of high velocity Endothelial damage Platelet-fibrin thrombi (Nonbacterial Thrombotic endocarditis) Mucosal surface damage - dental Microorganism adherence (BTE) Local vegetation EXTENSON , Perivalvular ,Destructive valve, fistula and embolization

8 Determining Risk of IE Cardiac conditions Type of Procedure

9 Cardiac Conditions – High Risk1
Old recommendation Prosthetic Valves (400x risk2) Previous endocarditis Congenital heart disease Complex cyanotic disease (Tetralogy, Transposition, Single Ventricle) Patent Ductus Arteriosus VSD Coarctation of aorta Valvular: not included as per now Aortic Stenosis/ Aortic Regurgitations Mitral Regurgitation Mitral Stenosis with Regurgitations 1Durack, et al. NEJM 1995 Mod Risk per 1997 AHA guidelines 2Steckleberg, et al. Inf Dis Clin N Amer 1993

10 2015 recommendations

11 2015 recomendations

12 Prophylaxis against IE ACC 2017
Is reasonable before dental procedures that involve manipulation of: gingival tissue, peri-apical region of teeth, or perforation of the oral mucosa in patients with the following: 1. Prosthetic cardiac valves, including trans-catheter-implanted prostheses & homografts. 2. Prosthetic material used for cardiac valve repair, such as annuloplasty rings & chords. 3. Previous IE. 4. Unrepaired cyanotic congenital heart disease or repaired congenital heart disease, with residual shunts or valvular regurgitation at the site of or adjacent to the site of a prosthetic patch or prosthetic device. 5. Cardiac transplant with valve regurgitation due to a structurally abnormal valve.

13 CLASSIFICATION OF ie Type of lesion Native. Congenital Prosthetic.
Onset & progress Acute. Sub acute. Acquire of infection Nosocomial . community

14 DIAGNOSIS OF IE Clinical suspension Blood culture Echocardiography

15 Clinical Features-1 › Indolent course: -fever - Malaise
Onset usually within 2 weeks of infection › Indolent course: -fever - Malaise - Fatigue - Night sweats - Anorexia - Weight loss › Explosive course: - CCF , murmur new onset or changing characters, with severe systemic sepsis

16 Other Clinical Features-2
Spleno-megaly ~ 30% Petechiae % Conjunctivae Buccal mucosa palate Skin in supra-clavicular regions Osler’s Nodes % Splinter Haemorrhages % Roth Spots ~ 5% Musculoskeletal (arthritis)

17 Vascular and septic emboli
Immonuligical Vascular and septic emboli Osler nodes Roth spot Gomeriolo-nephritis Rheomatoid factor + Splinter hemorrhage Janway lesion : painless skin lesion in the palm and sole. Sub-conjuctival hemorrhage Mycotic aneurysm Arthritis hematurea

18 Clinical features- immunological phenomina (glumerolo-nephriti, osler nodes, roth spot , RF +ve)
Osler nodes , painful lesion in distal finger

19 Roth Spots

20 Vascular Phenomina -Septic emboli
Janway , vascular Painless hemorrhagic cutaneus lesion in the palm and sole Splinter hg

21 Subconjunctival Hemorrhages

22 AA common mnemonic for the signs and symptoms of endocarditis is FROM JANE:
F- FEVER R- ROTH SPOT O- OSLER NODE M- MURMER J- JEANWAY LESION A- ANEMIA N- NAIL HG (SPLINTER HG) E- EMBOLI

23 INVESTIGATIONS C.B.C ESR Blood cultures RFT URINE ECG CXR ECHO

24 TEE

25 Skin most predominant source of infection
IE in IV Drug Abusers Skin most predominant source of infection % of Rt. sided IE results in pneumonia and septic emboli Microbiology Staph aureus ~60% Streptococci and Enterococci ~20% Gram -ve bacilli ~10% Fungi (Candida and Aspergillus ~5%

26 Prosthetic Valve Endocarditis Classification
Early ( < 60 days ) Reflects perioperative contamination Incidence around 1% Microbiology Staph ( %) Staph. Epiderm (~ 30%) Staph. Aureus (~ 20%) Gram -ve aerobes (~20%) Fungi (~ 10%) Strep and Entero (5-10%) Late ( > 60 days) After endothelialization Incidence % / pt. year Transient bacteraemia from dental, GI or GU Microbiology resembles native valve endocarditis

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29 DUKE CRITERIA BE-FEVEER(SUMMARY)
MAJOR B-BLOOD CULTURE +VE >2 TIMES 12 HOUR APART E- ENDOCARDIAL INVOLVEMENT FROM ECHO MINOR CRITERIA F- FEVER E- ECHO FINDING NOT MAJOR V- VASCULAR PHENOMINA EE- EVIDENCE FROM MICROBIAL /IMMUNOLOGICAL- 2 EVIDENCE R- RISK FCTOR FOR IE VALVE DISEASE /CONGEITAL DRUG ABUSER

30 Diagnostic (Duke) Criteria
Definitive infective endocarditis Pathologic criteria Microorganisms or pathologic lesions: demonstrated by culture or histology in a vegetation, or in a vegetation that has embolized, or in an intracardiac abscess Clinical criteria (as above) Two major criteria, or One major and three minor criteria, or Five minor criteria

31 Diagnostic (Duke) Criteria
Possible infective endocarditis findings consistent of IE that fall short of “definite”, but not “rejected” IE considered in presence of 1 major + 1 minor or 3 minor Rejected Firm alternate Dx for manifestation of IE Resolution of manifestations of IE, with antibiotic therapy for  4 days No pathologic evidence of IE at surgery or autopsy, after antibiotic therapy for  4 days

32 Treatment Medical – antibiotic Surgical

33 Principles of Medical Management
Antibiotic needs : prolonged , high dose and bactericidal. Acute onset: blood culture and start treatment within three hours. Sub acute onset ; Blood culture then antibiotic can be started within three days.

34 Treatment Pre-antibiotic era - a death sentence Antibiotic era
Microbiologic cure in majority of patient Highly penicillin-susceptible Streptococcus viridans or bovis Once-daily ceftriaxone for 4 wks cure rate > 98% Once-daily ceftriaxone 2 g for 2wks followed by oral amoxicillin qid for 2 wks Prosthetic valve may need longer treatment durations.

35 Complications-1 Congestive Cardiac Failure (Commonest complication)
Valve Destruction Myocarditis Coronary artery embolism and MI Myocardial Abscesses Neurological Manifestations (1/3 cases) Major embolism to MCA territory ~25% Mycotic Aneurysms %

36 Neurological Complication

37 Complications-2 Metastatic infections Rt. Sided vegetations
Lung abscesses Pyothorax / Pyo-pneumothorax Lt. Sided vegetations Pyogenic Meningitis Splenic Abscesses Pyelonephritis Osteomyelitis Renal impairment , Glomerulonephritis

38 Prevention

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41 Staphylococcus Flocloxacilline Or Vancomycine


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